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Annual Meeting Program Addendum
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View 44th Annual Scientific Meeting schedule changes and updates to the Abstract Supplement.  

 

Annual Meeting Program Addendum - Schedule Changes 

(confirmed after 30 July)

Thursday, 17 September 2015
10:15 – 11:45
SESSIONS 2: HEMATOPOIESIS I
Invited Speaker 3 unable to present: Atsushi Iwama, Chiba University, Japan (1004)
Invited Speaker 3 added: Atsushi Hirao, Kanazawa University; Japan (1041)
Molecular Mechanism Linking Hematopoietic Stem Cell Aging and Leukemogenesis

18:00 – 20:00
POSTER VIEWING & DISCUSSION I
Moved to Sakura
3057 – DECLINED PRESENTATION

 

Friday, 18 September 2015
16:00 – 17:30
SESSION 11B: CELL AND GENE THERAPY
Invited Speaker 1 unable to present: Philip Gregory, Sangamo BioSciences, Inc., USA (1025)
Invited Speaker 1 added: Edward Raber, Sangamo BioSciences, Inc., USA (1039)
Genome Engineering with Zinc Finger Nucleases
Invited Speaker 2 unable to present: Akiko Shimamura, Fred Hutchinson Cancer Research Center, USA (1026)
Invited Speaker 2 added: Ute Koch, École Polytechnique Fédérale de Laussanne, Switzerland (1040)
Dicer1 Imparts Essential Survival Cues in Notch Driven T-ALL via miR-21 Mediated Tumor Suppressor Pdcd4 Repression

17:30 – 19:30
POSTER VIEWING & DISCUSSION II
Moved to Sakura
3216 – DECLINED PRESENTATION


Saturday, 19 September 2015
9:00 – 10:30
SESSION 12B LEUKEMIA II
LBA Short Talk 2 added: Takahiro Ito, University of Georgia, USA (2014)|
Post-transcriptional Regulation of AML Propagation by Oncogenic RNA Binding Proteins

SESSION 13: SPONSORED LUNCH SESSION
Invited Speaker 2 added: Toshio Suda, Cancer Science Institute, National University of Singapore (1032) Hematopoiesis Under Stress


SESSION 14A: DEVELOPMENTAL HEMATOPOIESIS II
LBA Short Talk 2 added: Tiago Luis, University of Oxford, UK (2016)
Embryonic Thymopoiesis is Initiated by Immune-restricted Lympho-myeloid Progenitor Independently of Notch Signaling


SESSION 14B: XENOTRANSPLANTATION MODELS
LBA Short Talk 1 added: Ayano Yurino, Kyushu University, Japan (2017)
Kit Mutation Enhanced Human Megakaryo-erythroid Reconstitution in Xenotransplantation System

 

Annual Meeting Program Addendum - Abstract Supplement Updates

*denotes the change 


Thursday, 17 September 2015
10:15 – 11:45
SESSION 2: HEMATOPOIESIS I
1041 – MOLECULAR MECHANISM LINKING HEMATOPOIETIC STEM CELL AGING AND LEUKEMOGENESIS
Atsushi Hirao
Kanazawa University, Japan

 

Hematopoietic stem cells (HSCs) are maintained in an undifferentiated quiescent state within a bone marrow niche. Although appropriate intrinsic and extrinsic controls are required for HSC homeostasis, the underlying molecular mechanisms are still unknown. In order to maintain HSC homeostasis over the life of an animal, HSCs must either be long-lived or self-renew. In either case, the quality of HSCs must be sustained during aging so that these cells and their progeny are comparable to those derived from HSCs in a young animal. Although aging is a complicated phenomenon, its effects on HSCs have been dissected by examining molecules in the stress responses, DNA damage/repair processes, epigenetics, inflammation, cellular senescence and metabolism. We hypothesized that HSC fate may be controlled by molecules that are involved in nutrient signals, because it has been demonstrated that caloric restriction extends lifespan or restores aging phenotypes. Therefore, we focused on mTOR complex 1 (mTORC1) and forkhead transcription factor FoxO, which function in nutrient sensing signaling pathways. In the quiescent HSCs, the phosphorylation of AKT is down-regulated, associated with activation of FoxO3a. FoxO3a-deficient HSCs showed increased phosphorylation of p38MAPK, an elevation of ROS, defective HSC function during aging. Dysregulation of mTORC1 also causes abnormality in HSC behavior. Thus, appropriate controls of these signaling pathways play a pivotal role in maintaining the HSC homeostasis. In addition to nutrient signals, we have been investigating roles of a negative regulator of c-kit signals, Spred1, on HSC self-renewal and leukemogenesis. We found that Spred1 controls self-renewal activity and aging of HSCs. In this seminar, I would like to present recent data regarding how fine-turning of nutrient/cytokine pathways control HCS aging.
*abstract added

 

Friday, 18 September 2015

16:00 – 17:30
SESSION 11B: CELL AND GENE THERAPY
1039 - GENOME ENGINEERING WITH ZINC FINGER NUCLEASES
Edward Raber
Sangamo BioSciences, Inc., USA

 

Proteins that can be designed to cleave user-chosen sites in a living genome provide powerful tools for engineering eukaryotic cells with new and useful properties. By provoking break repair of the targeted locus, such proteins can mediate highly efficient rates of gene editing, gene disruption or gene addition at levels that allow ready isolation of cells or organisms bearing a desired genetic change. These capabilities have enabled diverse applications in research and biotechnology. They also offer the prospect of new strategies for treating disease in which patient cells are engineered ex vivo or in vivo to impart new, therapeutically beneficial properties.This talk will describe our recent applications of zinc finger nucleases to research and therapeutic challenges in hematology, with a focus on hemoglobinopathies and hemophilia. Specific examples will include the use of zinc finger nucleases to identify and disrupt a key enhancer element of BCL11A expression and to catalyze the integration of clotting factor transgenes into the albumin locus with amelioration of bleeding phenotypes in mouse models of hemophilia A and B. This talk will also provide a brief overview of the structure, design and targeting capabilities of zinc finger nucleases.
*abstract added


1040 - DICER1 IMPARTS ESSENTIAL SURVIVAL CUES IN NOTCH DRIVEN T-ALL VIA MIR-21 MEDIATED TUMOR SUPRESSOR PDCD4 REPRESSION
Ute Koch
École Polytechnique Fédérale de Laussanne, Switzerland

The modulatory function of individual miRNAs in Notch driven T-ALLs has recently been established. Although pro-tumorigenic and tumor-suppressive miRNAs are implicated in disease onset in murine models of Notch-driven T cell leukemia, whether Dicer1-processed miRNAs are essential for Notch-driven T-ALL is currently unknown. Here we used conditional and inducible genetic loss of function approaches to test whether the development and maintenance of Notch-driven T-ALL was dependent on Dicer1 function. Mice with specific inactivation of both Dicer1 alleles in the T cell lineage did not develop Notch-driven T-ALL. In contrast, loss of one functional Dicer1 allele did not significantly perturb T-ALL onset and tumor progression. Inducible inactivation of Dicer1 in early stage polyclonal T-ALL cells was sufficient to abrogate T-ALL progression in leukemic mice whereas late stage monoclonal T-ALL cells were counter-selected against loss of Dicer1. Lineage tracing experiments revealed that Dicer1 deficiency led to the induction of apoptosis in T-ALL cells whereas cell cycle progression remained unaltered. Through microarray-based miRNA profiling, we identified miR-21 as a previously unrecognized miRNA deregulated in both mouse and human T-ALL. Herein, we demonstrate that miR-21 regulates T-ALL cell survival via repression of the tumor suppressor Pdcd4.
*abstract added

Saturday, 19 September 2015
SESSION 13: SPONSORED LUNCH SESSION
1032 – HEMATOPOIESIS UNDER STRESS
Toshio Suda

Cancer Science Institute, National University of Singapore

The hematopoietic niche of the bone marrow provides a specialized microenvironment for the regulation of both steady-state hematopoiesis and stress hematopoiesis. HSCs are predominantly kept in a quiescent state to avoid exhaustion upon various stresses. Growing evidence has suggested that HSCs have unique characteristics in their DNA damage response owing to their quiescence.
In this presentation, I first will summarize our recent HSC niche studies, and then will focus on the hematopoiesis under stress, including infection and leukemia.
Regarding to hematopoietic response to infection, I will show that a bacterial second messenger, cyclic-di-GMP comprehensively regulates both HSPC and their niches cells through an innate immune sensor STING. This suggests that bacterial infection may drive sting signal pathway including nucleic acid receptors.
Regarding DNA damages and leukemia transformation, I would like to present the novel DNA damages response in HSCs. Avoiding accumulation of mutations which cause hematological diseases is substantive matter for maintaining HSC homeostasis. Using genetically altered mice, we demonstrate that apoptosis-stimulating protein of p53 1 (Aspp1) is a critical regulator of HSCs, which functions in coordination with p53. Aspp1-deficiency sustains HSCs self-renewal and enhances quiescence after serial transplantation, suggesting that Aspp1 counteracts stem cell ability in stressed conditions. Furthermore, Aspp1 sensitize HSCs to apoptosis after genotoxic stress, resulting in elimination of HSCs with persistent DNA damage. Finally, concomitant loss of Aspp1 and p53 leads to the transformation of hematological malignancies.
Each result respectively uncover function of DNA receptor signaling or DNA damage response from the aspect of the stress response. It is speculated that stress-induced DNA damage may be linked to a DNA receptor such as STING, which collectively insight into how HSCs manage to sustain their hematopoiesis under continued stress.
*abstract added


Thursday, 17 September
18:00 – 2:00
POSTER VIEWING AND DISCUSSION I
3087 – CD11B+CX3CR1+CELLS PLAY A DETERMINIG ROLE IN PREPARATIVE ANGIOGENSIS AFTER ISCHEMIC INJURY
Jeong-A, MD, PhD1,2, Kyoungmi Noh2, Joon Lee2, Youngrok Park4, and Hal E. Broxmeyer, PhD3, Jae-Yong Kwak, MD, PhD5

1Division of hematology, Department of Internal Medicine, The Catholic University of Korea, Seoul, South Korea; 2Cancer Research Institute, The Catholic University of Korea, Seoul, South Korea; 4Department of Molecular and Cellular Biology, Johns Hopkins University, Baltimore, MD; 3Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN; 5Department of Internal medicine, Chonbuk National University Medical School & Hospital, Jeonju, South Korea.
*author order

3141 – THE DYNAMIC INTERPLAY OF GATA ZINC-FINGERS IN BLOOD DEVELOPMENT AND DISEASE
Nurmohamed S. Broadhurst

RW, May GE, Enver T

Acute myeloid leukaemia (AML) is the most common type of blood cancer in adults. AML is highly malignant and most patients eventually die from the disease in spite of aggressive therapy. GATA2 is a transcription factor essential to blood-cell development; it is a master-regulator of stem and progenitor cell development. In order to regulate gene expression, it binds to DNA and simultaneously makes physical contacts with other regulatory proteins. Interruption of these interactions alters the behaviour of blood cell development and ultimately causes leukaemia. Using a multidisciplinary approach, we shed light on the dynamic interplay between the zinc-fingers and their protein/DNA binding-partners to elucidate the molecular mechanism of how GATA2 may function in haematopoiesis and disease.
*author and abstract change


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